Format

Send to

Choose Destination
See comment in PubMed Commons below
Med Sci Monit. 2013 Jan 9;19:28-33.

Ratio of angiopoietin-2 to angiopoietin-1 predicts mortality in acute lung injury induced by paraquat.

Author information

1
Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea.

Abstract

BACKGROUND:

To determine whether initial reactive oxygen species (ROS)-induced endothelial cell injury is involved in early death after paraquat intoxication and concentrations of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and von Willebrand factor (VWF) reflecting endothelial cell injury, we investigated the initial endothelial cell injury marker involved in the pathogenesis of death within 5 days after paraquat ingestion.

MATERIAL/METHODS:

Sixty patients with paraquat poisoning were prospectively enrolled. Plasma samples were collected at admission. Plasma concentrations of Ang-1, Ang-2, and VWF were measured by enzyme-linked immunosorbent assay. The patients were classified into 3 categories: survivors, early death (died within 5 days after ingestion), and late death (died more than 5 days after ingestion).

RESULTS:

The baseline concentration of Ang-2 and the Ang-2: Ang-1 ratio were significantly higher in patients who died (Ang-2 [pg/mL], 1012.75 ± 468.02 vs. 1986.07 ± 1675.37 [p=0.002]; Ang-2: Ang-1, 0.90 ± 0.49 vs. 2.16 ± 2.28 [p=0.002]). The Ang-2: Ang-1 ratio was significantly higher in the early death group (2.41 ± 2.54) than in the survivors (0.90 ± 0.49) and the late death group (1.33 ± 0.64). The Ang-2: Ang-1 ratio was significantly associated with early death (OR, 2.602; 95% CI, 1.106-6.117; p=0.028) after adjusting for plasma levels of paraquat, age, PCO2, and creatinine. VWF did not predict mortality.

CONCLUSIONS:

Endothelial cell damage could be involved in the pathogenesis of early death following paraquat ingestion.

PMID:
23302768
PMCID:
PMC3628933
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for International Scientific Literature, Ltd. Icon for PubMed Central
    Loading ...
    Support Center